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Department of Neurology and the Marine Biomedical Institute, University of Texas Medical Branch, Galveston, TX.
We examined the axonal transport of monoclonal IgM that binds to Thy 1.1, a glycoprotein component of the neuronal and synaptic plasma membrane, in the rat, using immunohistochemical techniques. IgM immunoreactivity appeared in neurons 1 to 2 days following injection in their terminal fields. Several neural pathways supported retrograde axonal transport of IgM, including facial nucleus, hypoglossal nucleus, and thalamic projections. Although the IgM studied had a greater affinity for Thy 1.1 than the IgG, IgM axonal transport was more difficult to detect than axonal transport of IgG, suggesting that IgM undergoes retrograde axonal transport less readily than IgG. An increase in intraneuronal IgM may serve as an index of the action of antineuronal IgM at the presynaptic membrane, and intraneuronal IgM may be directly involved in the pathogenesis of some types of motor neuron disease and neuropathy.
Address correspondence and reprint requests to Dr. Roderic H. Fabian, Department of Neurology, University of Texas Medical Branch Rt. E-39, Galveston, TX 77550.
Supported by NIH grant NS-11255.
Presented in part at the 41st annual meeting of the American Academy of Neurology, Chicago, IL, April 1989.
Received June 6,1989. Accepted for publication in final form August 23,1989.
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